2025/12/04 by Yumiko Chiba, Keiko Kaihara, Gentaro Iribe · 1 voice
Neuroscience · Biochemistry, Genetics and Molecular Biology · Medicine · #Ion Channels and Receptors #Connexins and lens biology #Cardiovascular Effects of Exercise
paper · doi:10.1016/j.jphyss.2025.100052
openalex created_date 2025/12/04 · openalex publication_date 2025/12/04 · openalex updated_date 2026/07/23
TRPC3 channels are involved in the physiological and pathological myocardial responses to mechanical loads. However, the involvement of TRPC3 in the response to acute stretch, that is, the Frank-Starling mechanism, has not been comprehensively elucidated. To elucidate this, we analyzed the response to stretch in isolated mouse ventricular cardiomyocytes. Our analysis revealed that TRPC3-deficient cells exhibited significantly lower cellular end-systolic elastance, an index of contractility, than wild-type cells owing to the absence of acute stretch-induced reactive oxygen species (ROS) production. Subsequently, we demonstrated that ATP released from pannexin-1 during stretch activates the TRPC3-NOX2 complex via P2Y signaling, thereby increasing ROS production. The results of this study show that TRPC3 plays a role in the Frank-Starling mechanism by mediating the mechanotransduction pathway of stretch-induced ROS production, which is a novel physiological role for TRPC3 in the heart.